Counterpoint: Standardization of Cardiac Troponin I Assays Will Not Occur in My Lifetime

I have chosen to address the argument of why cardiac troponin I (cTnI)3 assays will likely never be standardized. It is not that I do not wish it would happen, but I think the scientific, evidence-based story I will present regarding this cardiac specific protein will speak for itself. As a means to present this argument, I would like to consider the following analogy. I am an avid trail runner. During the second week of June, I set out every morning to run a 10-km rolling trail along the Ammonoosuc River in Bretton Woods, New Hampshire. Although the path I navigated each day was the same, what I observed each morning at 7 AM was dramatically different. It was influenced by the temperature, the wind, rain with thunder and lightning, puddles in rocky crevasses, tree branches covering the path, and, twice, minor course changes due to a fox and 2 black bears that appeared both upstream and downstream on the trail I was navigating. So, what does this analogy have to do with the cTnI story? cTnI, a protein of 110 amino acid residues with a unique N-terminal sequence that differentiates it from skeletal muscle forms, is part of the myofibril 3 subcomplex (cTnI–cTnC–cTnT) in the heart with specific structural and regulatory functions (1). Shortly after cell death caused by an acute myocardial infarction (MI), cTnI is released from the damaged myocardium into the extracellular space, and 1–6 h after onset of the index event, cTnI can be detected circulating in the blood (2). Data indicate that cTnI circulates mainly as a binary complex with cTnC in the blood of patients with acute MI, but it also circulates as free cTnI and as a ternary complex, cTnICT. In addition, C- and N-terminal proteolytic …